Scalp microbiome in male androgenetic alopecia: 16S rRNA sequencing-based clinical characterization, mouse model validation, and effects on hair follicle cells.

INTRODUCTION

Persistent microinflammation in androgenetic alopecia (AGA) may contribute to hair follicle miniaturization, but whether scalp microbial dysbiosis serves as its trigger remains unclear. This study integrated clinical samples, an animal model, and in vitro experiments to investigate the scalp microbiome in AGA.

METHODS

Scalp microbial samples were collected from four regions (frontal, vertex, temporal, occipital) of 12 AGA patients and 12 healthy controls (96 samples in total) and analyzed by 16S rRNA gene sequencing. An AGA mouse model was established using testosterone propionate to evaluate histopathology and skin microbiota. The effects of Staphylococcus epidermidis-derived phenol-soluble modulins PSMγ and PSMδ on human dermal papilla cell (HDPC) proliferation were assessed, and the effect of PSMδ on cell migration was also examined.

RESULTS

AGA patients exhibited elevated overall scalp microbial richness and diversity, with a marked decrease in Staphylococcus abundance that was most pronounced in the frontal and vertex regions. The mouse model also displayed significant restructuring of the skin microbiota; however, Staphylococcus showed marked enrichment-a direction opposite to that in humans. Together, these findings indicate that aberrant Staphylococcus abundance serves as a sensitive bio-indicator of the AGA pathological state. PSMδ significantly promoted HDPC proliferation in a time- and concentration-dependent manner, demonstrating a wider effective concentration window and milder action, and it also significantly enhanced cell migration.

DISCUSSION: The dysregulation of Staphylococcus abundance is a key feature of scalp microbial dysbiosis in AGA. PSMδ possesses dual potential in modulating hair follicle cell activity and maintaining microecological homeostasis, providing new insights for microbiome-targeted interventions in AGA.